Influence of platelet-activating factor receptor (PAFR) on Brucella abortus infection: implications for manipulating the phagocytic strategy of B. abortus
Lee et al. BMC Microbiology (2016) 16:70, DOI 10.1186/s12866-016-0685-8
Abstract
Background: Brucella abortus is an intracellular pathogen which can infect and persist in host cells through
multiple interactions. Above all, its interaction to host cell receptor is important to understand the pathogenic
mechanisms of B. abortus. Accordingly, we demonstrated that platelet-activating factor receptor (PAFR) affects
host cell response against B. abortus infection.
Results: First of all, B. abortus infection to macrophage induces secretion of platelet-activating factor (PAF), which is
a PAFR agonist. The stimulation of PAFR by PAF remarkably increases B. abortus uptake into macrophages. It induces
Janus kinase 2 (JAK2) and p38α phosphorylation, indicating that PAFR-mediated activation of JAK2 signaling leads to
enhanced uptake of B. abortus. Moreover, the dynamics of F-actin polymerization revealed that PAFR-mediated B.
abortus uptake is related with the reorganization of F-actin and JAK2. Upon B. abortus phagocytosis, reduced PAFR
in the membrane and subsequently increased levels of PAFR colocalization with endosomes were observed which
indicate that B. abortus uptake into macrophages allowed PAFR trafficking to endosomes.
Conclusions: This study demonstrated that PAFR has a compelling involvement in B. abortus uptake as a promoter
of phagocytosis, which is associated with JAK2 activation. Thus, our findings establish a novel insight into a receptorrelated
phagocytic mechanism of B. abortus.
Keywords: B. abortus, Platelet-activating factor receptor, JAK2, Phagocytosis